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AIDS: 31 July 2010
van de Laar, Thijs JW; Matthews, Gail V; Prins, Maria; Danta, Mark aCluster of Infectious Diseases, Public Health Service, Amsterdam, The Netherlands bViral Hepatitis Clinical Research Program, National Centre for HIV Epidemiology and Clinical Research, University of New South Wales, Sydney, Australia cDepartment of Internal Medicine, Centre for Infection and Immunity Amsterdam, Academic Medical Centre, University of Amsterdam, Amsterdam, The Netherlands dSt Vincent's Clinical School, Faculty of Medicine, University of New South Wales, Sydney, Australia.

Introduction

Hepatitis C virus (HCV) was first identified in 1989 as the principal cause of posttransfusion non-A non-B hepatitis [1]. Worldwide an estimated 170 million people are infected with HCV; due to shared routes of transmission, 4-5 million are coinfected with HIV [2]. HCV is usually transmitted parenterally. Within high-income countries, HCV transmission through blood products has effectively been halted, leaving injecting drug use (IDU) as the major cause of new HCV infections [3]. In medium and low-income countries, however, iatrogenic HCV transmission still accounts for a significant proportion of incident infections [4].

Permucosal sexual transmission of HCV remains controversial. Differences in sexual orientation and risk behaviour of the study population; study design; the presence of unmeasured parental routes of HCV transmission; and the use of molecular epidemiological techniques to confirm transmission between partners, might explain conflicting results [5]. Anti-HCV prevalence rates up to 28% have been reported among spouses of HCV-infected individuals, increasing with relationship duration [6-8]. However, sexual transmission has often been ruled out using molecular typing [9-11]. Even when molecular typing confirmed a common source of infection, other possible routes of transmission within the household could not be excluded [12]. Based on prospective cohort studies, sexual transmission of HCV is relatively rare in monogamous heterosexual relationships and varies from 0 to 0.6% per year [13-16]. A slightly higher risk, 0.4-1.8% per year, has been reported for heterosexuals with multiple partners or those at risk for sexually transmitted infections (STIs) [5].

Since 2000 outbreaks of acute HCV among HIV-positive men who have sex with men (MSM) who denied IDU have been reported from Europe [17-22], the United States [23-25] and Australia [26]. Remarkably, the majority of HCV infections were related to permucosal rather than parenteral risk factors, reopening the discussion on the importance of sexual transmission. This review will synthesize the most recent epidemiological, immunological and management issues that have emerged as a result of the epidemic of acute HCV among HIV-infected MSM. Studies were identified by MEDLINE using appropriate keywords and supplemented with perusal of reference lists of relevant publications and abstracts of recent relevant conferences.

Epidemiology of hepatitis C virus in men who have sex with men

Hepatitis C virus prevalence

In early cross-sectional studies, anti-HCV prevalence among MSM ranged from 0 up to 23%, which was higher than that observed among voluntary blood donors and heterosexuals at risk for STI (reviewed in [3], [27-29]). However, many of these studies did not incorporate information on IDU. The studies that did, revealed an anti-HCV prevalence of 1-7% among MSM who denied IDU versus 25-50% among MSM with a history of IDU [20,30-32]. HCV prevalence was also consistently higher in HIV-positive MSM (3-39%) than MSM without HIV (0-19%) [20,30,31,33-35]. It was concluded that IDU was responsible for the majority of HCV infections in MSM and that HIV might play a role in HCV transmission.

Recent outbreaks of HCV among HIV-positive MSM who denied IDU in Europe, USA and Australia suggest sexual transmission of HCV [17-24,26]. A study from the UK showed that acquisition of HCV in MSM with primary HIV infection increased from 0% in 1999 to 4% in 2006 [36]. In the Netherlands, a bi-annual cross-sectional survey among STI-clinic attendees showed an alarming increase in HCV prevalence among HIV-infected MSM from 15% in 2007 to 21% in 2008, compared to an estimated HCV prevalence of 1-4% before 2000 [37]. Only 5% of HIV-positive MSM reported IDU, and a relatively high proportion was diagnosed with acute HCV infection. In contrast, a large study among 2268 HIV-infected MSM in Europe who were recruited between 1995 and 2003 showed a HCV prevalence of 6.6% [38], which is in line with the HCV prevalence observed at the beginning of the HIV epidemic. The HCV prevalence among HIV-negative MSM who deny IDU is low and comparable to that of the general population [37,39-41].

Molecular epidemiology

HCV sequencing data of HIV-positive MSM recently diagnosed with acute HCV in Europe show 90% are infected with difficult-to-treat HCV genotypes 1a and 4d [18-21,53]. Phylogenetic analysis revealed robust monophyletic transmission clusters of HCV within the MSM populations of major cities in England, France, the Netherlands and Germany [20-22,54]. An international collaborative study confirmed the presence of one large European MSM-specific transmission network, linking the independently reported outbreaks in London, Paris, Amsterdam and Berlin [55]. Based on the reported risk factors from the individual cohorts, this appears to be a sexual network. Evolutionary analysis based on the genetic divergence within MSM-specific HCV strains of genotype 1 and 4 in Europe suggests multiple independent introductions of HCV into the MSM community, some as early as the 1980s [20]. Most likely, these strains were introduced from the IDU population [20,37].

Molecular clock analysis suggests that this expansion of these MSM-specific HCV strains increased after 1996 [21,55]. Interestingly, this sudden emergence in HCV coincides with a rise in sexual risk behaviour and increased STI rates among MSM due to a decrease in the perceived threat of HIV/AIDS in the cART era [56-58]. The fact that multiple strains of different HCV genotypes circulate among HIV-positive MSM also suggests behavioural factors in the MSM population rather than evolution of the virus into a specific more virulent variant are responsible for the recent transmission of HCV in this population [55].

Phylogenetically, the HCV outbreak in Australia shows very limited overlap with the network that exists in Europe [55]. In Australia, approximately 50% of acute HCV infections among HIV-positive MSM are attributable to IDU, which might explain why HCV genotype 3a is more prevalent among Australian MSM (33%) than European MSM (7%) [26]. HCV strains obtained from Australian HIV-positive MSM do show a high degree of phylogenetic clustering. Robust monophyletic clusters of MSM-specific HCV strains were identified, in which there is mixing of sexually and IDU-acquired HCV [59]. In the United States, HCV genotype 1a predominates among HIV-positive MSM; however, no information on MSM-specific clustering is available yet [60].

What are the risk factors for hepatitis C virus transmission in men who have sex with men?

Early studies carried out among MSM in Sydney, San Francisco, Pittsburgh and Amsterdam indicated that HIV infection and IDU were independently associated with presence of HCV antibodies [20,30,31,34]. In univariate analysis, the evidence for sexual transmission was weak with some studies describing associations between HCV infection and sexual risk behaviour, such as unprotected anal intercourse, fisting, enema use and STI [31,34,35,42], whereas others did not [20,61-63]. Since the recent outbreak of HCV among HIV-positive MSM, two longitudinal cohorts [44,51], one cross-sectional study [37] and one case-control study [21] have examined the independent relationship of sexual risk behaviour with HCV, by comparing sexual risk behaviour of HCV-infected and HCV-uninfected MSM. In the prospective Swiss cohort study, unsafe sex and syphilis infection were significantly associated with acquiring HCV among MSM without a history of IDU [44]. However, limited data on specific sexual risk behaviours were available in this study. Only fisting remained associated with HCV in multivariate analysis of a longitudinal cohort of MSM attending the STI clinic in London [51]. However, risk behaviour was collected at baseline making it difficult to imply causal effects. A cross-sectional study from Amsterdam found that HIV infection, IDU, fisting and noninjecting recreational drug use, especially the use of gamma hydroxyl butyrate (GHB), were independently associated with HCV infection [37]. As this study was conducted among MSM with prevalent HCV infection, the actual HCV transmission event might have considerably preceded reported risk behaviour. Only one case-control study, HIV/HCV coinfection versus HIV monoinfection, explicitly investigated sexual risk factors and drug use among MSM diagnosed with acute HCV [21]. Although limited by a retrospective design, it suggests that permucosal traumatic sexual techniques, particularly when practised in the context of group sex and/or noninjecting recreational drug use, were associated with acute HCV infection [21]. These studies underline, however, that most MSM with HCV report a combination of various, potentially high-risk, sexual and drug practices. The interaction between sex and drugs is complex, and many of these factors are highly correlated and difficult to disentangle. Intranasal and rectal drug use in itself could favour HCV transmission via shared contaminated implements. It is more likely, however, that the association with drug use reflects residual confounding: unmeasured sexual risk behaviour due to disinhibition and sexual arousal. Based on current knowledge, sexual transmission of HCV is probably mediated by factors such as traumatic sexual techniques and ulcerative STI that may cause mucosal damage in the rectum. Nevertheless, acute cases of HCV have been described among MSM that deny all risk factors mentioned above.

Immunology and natural history

It is striking that the recent outbreak almost exclusively affects HIV-infected MSM. The natural history of HCV is determined by host-viral interactions, which are perturbed in HIV coinfection, resulting in accelerated liver fibrosis, higher HCV loads and poorer responses to interferon-based therapy when compared with HCV monoinfection [64]. Critical to an understanding of the HCV natural history is an understanding of early immunological control and clearance of HCV, and how HIV infection may affect this.

What constitutes a successful immune response to hepatitis C virus?

The emerging consensus is that early control and clearance of HCV infection is the result of a strong cellular immune response accompanied by innate mediators [65]. In the absence of HIV, approximately 25% of individuals will spontaneously clear HCV infection, whereas others have persistent infection marked by ongoing viraemia [66]. A successful immune response to HCV requires strong, broad, early and sustained HCV-specific CD4 and CD8 T-cell responses, in particularly directed against the nonstructural proteins [67-71]. Although most individuals mount measurable CD4 and CD8 T-cell responses, patients who failed to clear HCV either did not mount CD4 T-cell responses or, after initial virological control, do not sustain these responses with a subsequent relapse of HCV [68]. Chimpanzee studies have also demonstrated a loss of control of HCV related to depletion of CD4 and CD8 T cells [72,73]. HCV-specific T-cell responses were persistent and have been detectable up to two decades following resolution of HCV in a group of women who had been infected from human rhesus immunoglobulin [74].

There are a number of hypotheses as to how HCV evades these cell-mediated responses that have recently been reviewed [65]. The concept of T-cell exhaustion postulates that persistent stimulation of lymphocytes with high-level antigenaemia in HCV leads to reduced T-cell responses and apoptosis. Interestingly, this may be mediated by an inhibitory molecule programmed death-1 (PD-1). Furthermore, in HIV infection, exhaustion of CD8 T cells has been shown to occur following loss of CD4 T cells [75]. Another proposed mechanism may be induction of T-regulatory cells that inhibit antigen-specific T cells, such as CD8 T cells in HCV [76]. Finally, the rapid mutation of HCV has been shown to lead to escape mutation within specific CD8 T-cell epitopes [77,78].

Recently, there has been great interest in polymorphisms in the interleukin (IL) 28B gene on chromosome 19, which has been shown to predict spontaneous clearance and sustained virological response to combination HCV treatment [79,80]. The different racial distributions of this polymorphism may explain some of the racial differences in response to HCV treatment. There is also evidence that in HCV infection, there is a delayed cytokine responses when compared with other chronic viral infections such as HIV [81].

What is the impact of HIV on the immune response to acute hepatitis C virus?

In HIV coinfection, the rate of spontaneous clearance is significantly lower than that in HCV monoinfection, with reported rates ranging from 5 to 24% [82-84]. Furthermore, the viral set point is increased in HIV infection with one large cohort demonstrating an HCV load more than 1 log higher than that of HCV monoinfected individuals [83]. In chronic HCV infection, HIV-positive men are more likely to shed HCV RNA in semen than their HIV-negative counterparts [85]. Interestingly, the humoral response to HCV appears to be delayed in HIV infection. In a London cohort of 43 HIV-positive individuals with acute HCV, the proportion who had a negative HCV antibody results was 37, 10 and 5% at 3, 9 and 12 months after their first HCV RNA positive test result, respectively [86]. As a result, some have suggested that HCV-RNA testing should be performed for screening high-risk populations.

The poor control of HCV is the result of HIV's impact on the cell-mediated immune responses. It is clear that in chronic coinfection, HIV significantly impairs the cell-mediated responses to HCV antigens [87]. A large study of chronic HCV/HIV coinfected individuals found that lower CD4 cell counts were associated with reduced CD8 T-cell responses [88]. A UK cohort analysed immune responses in the acute phase of HCV infection, demonstrating that the immune defect to HCV occurs early in established HIV coinfection, even in individuals with relatively preserved CD4 cell counts (>500 cells/±l) [83]. Recently, a prospective French study of acute HCV cell-mediated responses in HIV coinfection demonstrated low frequency interferon gamma and weak HCV-specific memory T-cell responses [84].

Chronic HCV/HIV coinfection is associated with more rapid liver fibrosis with an estimated fibrosis progression rate of 0.15 versus 0.11 fibrosis units per year for HCV monoinfection [89]. Data are now emerging that acquisition of HCV following HIV may be associated with accelerated fibrosis [23,90]. In a small prospective series of 11 patients, nine (82%) had grade 2 liver fibrosis on liver biopsy [23]. This is a higher rate than has been reported in acute HCV monoinfection. In a recent immunological review of HCV and HIV coinfection [91], a number of potential mechanisms contributing to accelerated liver fibrosis were described, including altered cytokines, increased hepatocyte and lymphocyte apoptosis, and increased oxidative stress; bacterial translocation with increased levels of lipopolysaccharides (LPS); and external factors such as steatosis, insulin resistance and hepatotoxicity associated with antiretrovirals.

It is also likely that the immunological changes associated with HIV are contributing to the changing epidemiology in HIV-positive MSM. Although high-risk behaviours are certainly associated with transmission, there are specific immunological mechanisms that may also be contributing. First, HIV perturbations of the gastrointestinal immune system have become a major focus for the immunopathogenesis in HIV [92]. The compromised mucosal barrier, associated with viral replication and CD4 T-cell destruction, with consequent bacterial translocation are thought to be major drivers of AIDS progression. Although it has not yet been elucidated, it is conceivable that defects in mucosal immunity are also facilitating permucosal transmission of HCV. In addition, defects in cell-mediated responses are associated with reduced HCV clearance [92,93] and higher HCV viral loads in serum [94] and semen [85].

Treatment of acute hepatitis C in HIV-positive individuals

Chronic HCV is generally a slowly progressive disease with cirrhosis estimated to occur in up to 20% of individuals over a 40-year period [95]. Even in HIV-infected individuals, in whom disease progression is accelerated [96], end-stage liver disease is unlikely to occur in less than 5-10 years after initial infection [97]. The rationale, therefore, for treating HCV in the acute stages of infection is based on evidence suggesting that early treatment of acute HCV results in higher rates of sustained virological response (SVR) than treatment in established chronic HCV, presenting a window of therapeutic opportunity. In a seminal paper, Jaeckel et al. [98] reported 44 HIV-negative patients with acute HCV who were treated with standard interferon therapy for 24 weeks leading to an SVR of 98%. No subsequent study has managed to confirm such high rates of SVR in acute HCV infection, despite the introduction of pegylated interferon (PEG): SVR rates remain higher than those in chronic hepatitis C [at least for HCV genotype 1 (HCV-1) infections] at between 71 and 94% [99-103] versus 40 and 50% in chronic HCV-1 [104,105]. However, these studies were heterogeneous with regard to the populations studied, delay before commencement of treatment and duration of therapy. Large randomized clinical trials on the optimal treatment of acute HCV are difficult to perform, due largely to difficulties in identifying incident cases and in accurately assessing the timing of infection. Consequently, there remain many areas in which the guidelines for treating acute HCV are not yet fully evidence-based. This is particularly true of acute HCV in HIV-positive individuals in whom there is even greater uncertainty around optimal management. To date, published data on treatment outcomes in this setting are limited to 10 studies reporting HIV-positive individuals using various study designs and treatment regimens [22,24,50,53,82,106-110] (Table 2). SVR ranged from 0 to 91% [53] across studies, with most studies reporting rates between 60 and 80%. The treated French, UK and German cohorts (n = 150) were recently combined with a reported overall SVR of 62% [111]. Given that the predominant genotype was 1 or 4 in all these studies, this would support the theory that in HIV-positive, as in HIV-negative populations, treatment in the acute phase of HCV is indeed more successful than treatment in chronic HCV.

When to start treatment for acute hepatitis C virus in HIV-positive individuals?

Although HIV-infected individuals are less likely to spontaneously clear acute HCV infection than HIV-negative individuals, spontaneous eradication can occur [66,82-84,112]. It is still not clear how long should a patient be observed to allow for this possibility before commencing therapy. In a randomized study of acute HCV monoinfection in Egypt, SVR rates were compromised by a delay in start of PEG to 20 weeks from time of first positive HCV-RNA test result (76% SVR), but were similar in those starting 8 (95% SVR) or 12 (92% SVR) weeks after diagnosis [101]. The majority of patients in this study were infected through occupational exposure and it should be noted that in this study, a short duration of 12 weeks of treatment only was used. In HCV monoinfection, a 'watch and wait' policy of 12 weeks before commencing treatment is advised, and current guidelines on HIV-positive individuals similarly recommend waiting 12 weeks from estimated date of exposure to ensure that spontaneous clearance does not occur [113]. Recently, a week 4 HCV-RNA drop of more than 2 logs has been identified as a predictor of spontaneous viral clearance, which suggests early treatment could be targeted [114].

Is there an advantage of combination HCV therapy over monotherapy?

In HIV-negative individuals, acute HCV is almost always treated with PEG monotherapy as SVR rates have been typically high with these regimens. Only one study in this population has reported a comparison between PEG monotherapy and PEG in combination with ribavirin (RBV) finding no significant benefit of using combination therapy [102]. In HIV-positive individuals, there has been much greater variation in the regimens employed, with a general trend towards the use of combination rather than PEG monotherapy and guidelines now recommend the use of standard PEG/RBV combination for 24 weeks in HIV-positive individuals [113]. However, there is a paucity of evidence to support this. In three of the seven studies, the protocols were amended to combination therapy, either after an initial two patients failed treatment with PEG monotherapy [82] or as a consequence of another study that reported a high overall SVR rate of 91% and used PEG/RBV in five of 11 HIV-positive individuals with acute HCV [53]. In fact, in the subsequent German study, which used PEG/RBV in 21 participants and PEG monotherapy in 15 participants, there was no benefit observed with the addition of RBV [108]. Finally, dosing of RBV was inconsistent in these studies, making interpretation of effect difficult. In summary, there is very little evidence that RBV enhances treatment outcomes in this setting and may add significant risk of toxicity and drug interactions.

What is the optimal duration and monitoring of therapy?

Increasing attention has been given recently to the possibility of shortening the duration of therapy in acute HCV in HIV-negative individuals to 12 weeks. A number of studies on HIV-negative patients have examined this issue with encouraging results [103,115,116]. One study using 12 weeks of therapy with PEG monotherapy resulted in SVR more than 90%, provided therapy was initiated within 12 weeks of infection. No study on HIV-positive patients has reported outcomes with short-course therapy. The utility of early virological response monitoring in the HIV setting has been reported in one study only. In 20 HIV-positive patients treated for 24 weeks in the Australian Trial in Acute Hepatitis C (ATAHC) study, rapid virological response (RVR) was observed in 44% of individuals and had 100% positive predictive value for SVR [107]. Conversely, lack of early virological response (EVR) at week 12 may be an important predictor of nonresponse to therapy.

Due to the small numbers in the published studies, identification of predictors of response is very difficult. Until recently, HCV genotype has been recognized as the strongest predictor of successful treatment in chronic HCV monoinfection. No single treatment study has been able to demonstrate an effect of genotype on treatment outcome of acute HCV in HIV-positive patients, probably due to small numbers. The majority of participants were infected with HCV genotype 1 or 4 and had an overall SVR rate of 57% (Tables 2 and 3). This compares to an overall SVR rate of 87% in genotype 2/3 participant and suggests that there may be an effect by genotype on treatment response similar to that observed in chronic HCV infection. Recently, polymorphism of IL28 has been identified as the most important predictor of treatment response in HCV. Interestingly, a German group has recently reported no IL28 impact on treatment of acute HCV/HIV coinfection [117], whereas two other studies did report improved SVR with IL28 C/C alleles in chronic coinfection [117,118]. Furthermore, polymorphisms in both IL6 and tumour growth factor (TGF) have also been correlated with treatment outcome in acute HCV/HIV coinfection [119,120].

Discussion

Given the burden of liver disease, in particular HCV, on the morbidity and mortality in HIV patients in the cART era, the rapid and significant rise in the incidence of HCV in HIV-infected MSM living in high-income countries is alarming [121-123]. A significant change in the epidemiology of HCV has occurred, with HCV emerging as a STI among HIV-positive MSM [124]. The molecular phylogenetic studies have been important for providing robust evidence of common source transmission, in particular, demonstrating the existence of a large international transmission network in Europe. The molecular work implies, through identification of different genotypes and subtypes of HCV in this network, that the recent transmission is not the result of the HCV becoming more virulent, but more likely the result of other factors such as behavioural change. Work to date suggests that this permucosal HCV transmission results from high-risk sexual and non-IDU drug behaviours [21,37,44,51]. However, the complex interaction between these risks has not yet been fully elucidated. Based on our current knowledge, permucosal transmission of HCV is probably mediated by factors such as traumatic sexual practices and ulcerative STI that may cause mucosal damage in the rectum. The characterization of the precise mechanisms and risk factors will have to involve qualitative studies of transmission events and attitudes, in addition to the quantitative studies that have been done to date. As MSM-specific HCV strains in Europe are almost exclusively of difficult-to-treat HCV genotypes 1 and 4, a virological component cannot entirely be excluded. In particular, when we assume multiple introductions of HCV from the IDU population into the MSM population, the absence of genotype 3a, which is highly prevalent among European injecting drug users, remains unexplained.

The emergence of HIV as an STI has been limited to HIV-positive MSM [20,41]. The central role of HIV could relate to behavioural and biological factors. Interestingly, the data suggest that the HCV incidence in HIV-infected MSM has increased significantly following the introduction of cART and the subsequent rise in sexual risk behaviour and STI in the late 1990s [17,45,47,49,51,124]. This, however, cannot explain why there is no evidence for permucosal transmission of HCV in the 1980s, a period in which STI and sexual risk-taking were highly prevalent among MSM. As a result of the increased life expectancy of people living with HIV/AIDS and the ongoing transmission of HIV among MSM, the recent increase in permucosal HCV transmission could relate to changing sexual behaviours in the context of an increasing pool of HIV-infected MSM. The current HIV prevention strategy of serosorting, whereby MSM of concordant HIV status have negotiated unprotected sex, might be an important factor. In a review of changing MSM behaviours after the introduction of cART, serosorting, wherein MSM of concordant HIV status have unprotected sex, has become more prevalent and is certainly contributing to higher risk behaviours [125]. Although serosorting prevents HIV transmission, it does not prevent other STIs. In line with this review, several studies have suggested that internet and travel behaviour might be associated with the recent spread of HCV among HIV-positive MSM [21,37]. Of concern is the potential bridging of HCV transmission from the HIV-positive into the HIV-negative MSM population. Only one epidemiological study suggests potential bridging between HIV-positive and HIV-negative MSM [47], but as discussed before, this study has serious limitations. Molecular HCV data obtained from HIV-positive and HIV-negative MSM in the Australian ATAHC study revealed that a small proportion (6%) of HCV sequences obtained from HIV-negative MSM were part of MSM-specific clusters [59]. In conclusion, sporadic transmission from the HIV-positive population might occur, but currently the HCV incidence is low among HIV-negative MSM and the majority of HCV infections appear to be of an unrelated source, mostly IDU [20,37,41,59]. However, temporal trends in acute HCV infections in HIV-negative MSM should be closely monitored to allow timely initiation of interventions to prevent transmission in this group.

Biologically, there are a number of potential mechanisms related to HIV that might result in enhanced infectivity and susceptibility to HCV, including increased HCV loads in serum and semen [83,85] and defects in the gastrointestinal immune system [92]. The cell-mediated immune lesions leading to increased chronicity and higher HCV loads probably also contribute to the changing epidemiology of HCV and complicate its management. It is not yet known whether lower CD4 cell count increases the risk of acquiring HCV, but the fact that many MSM with acute HCV have relatively preserved CD4 cell counts suggests this may not be a critical factor. Although permucosal HCV transmission is probably occurring across gastrointestinal mucosa in these individuals, the specific immune defect in the mucosal cell-mediated immunological control mechanism localized in the gastrointestinal tract has not been identified [92]. Further studies, exploring prospective serum and semen HCV load in acute infection with HIV parameters and comparing HIV characteristics, including cART use between HIV-infected MSM with and without HCV would inform the importance of HIV and identify factors that could be used to reduce infection. Alternatively, it is plausible that HIV is transmitted more efficiently sexually compared to HCV, and hence in the vast majority of MSM who engage in high-risk sexual behaviour with HIV-positive MSM, acquisition of HIV will, therefore, precede HCV infection [36]. As studies on the impact of HCV on HIV outcome have predominantly been conducted in injecting drug users and haemophiliacs in whom HCV usually preceded HIV infection, future studies should also investigate the impact of HCV on HIV progression in this new group of coinfected MSM who acquired their HCV infection after HIV infection and at an older age. In particular because it might be associated with accelerated liver fibrosis [23,90].

Currently, the management of acute HCV in HIV-infected patients is based on experience of retrospective studies and data from HCV monoinfection studies. Recently, a large prospective study enrolling both HIV-infected and HIV-uninfected individuals with recently acquired HCV infection reported a 74% SVR rate after 24 weeks of PEG/RBV combination therapy in coinfected participants, higher than that in the monoinfected participants. These data suggest that early treatment was efficacious in this group and should be considered irrespective of HCV genotype and baseline HCV-RNA level [126]. With the development of the specifically targeted antiviral therapies for HCV (STAT-C), there will be a paradigm shift in our approach to treatment of HCV. HCV protease and polymerase inhibitors are currently in trial and appear to be highly efficacious [127]. There are also now study protocols that use a combination of STAT-Cs without an interferon backbone with encouraging preliminary results [128]. There is no doubt that this new class of antiviral therapies will have an important role in the future management of acute and chronic HCV/HIV coinfection. However, the majority of the STAT-C agents in development are targeted at genotype 1 HCV infection, though a significant proportion of the recent HCV in HIV has been nongenotype 1. Therefore, in the short-term, PEG with or without RBV will remain the standard of care. Given this, it is important to be able to stratify individuals to treatment. As outlined, there is some emerging data on the use of early viral kinetics, such as week 4 HCV-RNA in predicting spontaneous clearance and SVR. In addition, other markers such as IL28b polymorphisms may become valuable predictors of HCV spontaneous clearance and response to interferon-based treatments. The role of individualizing treatment is incomplete, in part because of the piecemeal way the case series have been reported. Factors such as the specific therapy, timing and length of treatment in this population should ideally be addressed within appropriately powered randomized clinical trials. At the very least, large international collaborations that combine data across cohorts in a consistent manner are important to establish.

Targeted prevention such as raising awareness, regular screening and treatment of acute and chronic infections are needed to stop the further spread among MSM. Very limited data are available on HCV in MSM in middle and low-income countries. A hallmark of the successful HIV/AIDS response has been the underpinning of HIV education and prevention by sound epidemiological data. Although these issues are complex, improving our understanding of the risk behaviours and attitudes would help public health interventions to be appropriately focused. HCV education and prevention materials for MSM have already been developed based on current data and implemented in countries such as UK and the Netherlands. It is clear that a message of 'safe sex' through condom use during anal intercourse could be provided, but given the practice of negotiated unprotected sex among HIV-infected MSM might not be accepted. In addition, it may not cover practices that increase risk of blood-to-blood contact (e.g. fisting). Furthermore, MSM population needs to be informed that reinfection is an ongoing risk, given the recent reports of HCV reinfection following successful treatment and documented clearance of HCV [129]. Characterization of biological factors not only has implications for the MSM population involved in unprotected anal intercourse, but may also have implications for the wider HCV/HIV coinfected population [130]. Recognition of the current problem should lead to collaborative efforts to identify strategies to mitigate and manage this important growing problem.

However, HCC treatment resulted in similar overall survival rates in patients with undetectable and detectable serum HIV-RNA levels.

These were the findings of a study presented on July 21 here at the 18th International AIDS Conference by Emma Page, MD, Liver Cancer in HIV Study Group, Chelsea & Westminster Hospital, London, United Kingdom.

Among the 115 patients analysed in the study, median overall survival was longer in the group with undetectable HIV-RNA (11.7 vs. 4.9 months; P = .007). However, increased survival benefit was seen only in patients with undetectable HIV-RNA who were untreated for HCC (6.4 vs 2.5 months; P = .005).

The median overall survival in patients with any effective HCC therapy was 12.7 months and 9.3 months, in the HIV-RNA undetectable and detectable groups, respectively (P = .74).

Researchers analysed data from 115 patients with HIV and HCC who were seen from 1992 to 2009 in 22 centres throughout North and South America and Europe who had results of HIV-RNA testing available at time of HCC diagnosis.

(SACRAMENTO, Calif.) — MediCal patients may be taking dangerous amounts of acetaminophen, according to new research from UC Davis. Published in the July/August issue of the Annals of Pharmacotherapy, the study showed that the analgesic, generally considered safe at four grams a day or less, is prescribed to some patients in quantities far exceeding that guideline.

“Although small, the number of patients who could have taken 16 grams or more for at least one day is very concerning,” said lead author Timothy Albertson, acting chair of internal medicine for UC Davis Health System, “and the fact that many patients had total prescriptions that could have resulted in more than 100 days of four grams per day or more is truly alarming.”

Commonly sold over the counter under the brand name Tylenol, acetaminophen is one of the most popular pain-relief medications worldwide. It is frequently included in over-the-counter cold treatments and with prescription medications, making it easy for consumers to reach the four-grams-a-day or higher mark. Multiple case reports have suggested that four to six grams per day — especially if taken over time or in combination with alcohol — may induce liver or kidney damage in healthy and vulnerable patients alike.

“We have to be concerned about prescriptions for pain relief because nearly all of them contain acetaminophen, and it’s possible that significant amounts will be consumed daily or over the course of a few days,” said Albertson. “Better systems and stronger education of patients, prescribers and pharmacists are needed to reduce potential toxic exposure.”

Albertson and his team examined pharmacy claims within California’s Medicaid (known as MediCal) program for medications, including over-the-counter medications, that could result in acetaminophen doses exceeding four grams per day. They found that during 12 months in 2004 and 2005, an average of about 3.27 million beneficiaries were enrolled in the MediCal program and 961,320 of them, or 29.4 percent, received one or more prescriptions that included acetaminophen. If taken as directed, a total of 192,716, or 5.9 percent, were exposed to at least one day of acetaminophen doses exceeding four grams per day. Of those, 769 patients were potentially exposed to at least one day of 16 grams per day or more, and 2,664 beneficiaries were exposed to 100 days or more of acetaminophen doses of four grams per day or more.

Sixty-one patients with claims for four grams per day or greater of acetaminophen for more than 100 days had a diagnosis of primary liver or renal dysfunction, which the study team also found to be alarming.

Albertson pointed out that a recent Food and Drug Administration advisory committee recommended reducing the maximum total daily dose of acetaminophen and increasing outreach to health-care providers and consumers about the risks of overdose. To reduce the potential for over-prescribing the medication, he and his research team also recommend:

•Conducting additional research to investigate the link between chronic high-dose acetaminophen exposure and an increased risk of acute or chronic liver or kidney disease.

“Acetaminophen has provided a good pain-relief alternative, especially for those who are unable to take medications like aspirin due to stomach irritation,” said Albertson. “But that doesn’t mean that it is safe in all instances or in all amounts. We need to be just as careful with this medication as we are with others.”

A copy of “A Population Study of the Frequency of High-dose Acetaminophen Prescribing and Dispensing” can be downloaded at http://www.theannals.com./

The UC Davis School of Medicine is among the nation's leading medical schools, recognized for its research and primary-care programs. The school offers fully accredited master’s degree programs in public health and in informatics, and its combined M.D.-Ph.D. program is training the next generation of physician-scientists to conduct high-impact research and translate discoveries into better clinical care. Along with being a recognized leader in medical research, the school is committed to serving underserved communities and advancing rural health. For further information, visit the UC Davis School of Medicine website.

In recent years, scientists have shown that they can reprogram human skin cells to an immature state that allows the cells to become any type of cell. This ability, known as pluripotency, holds the promise of treating diseases such as diabetes and Parkinson's disease by transforming the patients' own cells into replacements for the nonfunctioning tissue.

However, the techniques now used to transform cells pose some serious safety hazards. To deliver the genes necessary to reprogram cells to a pluripotent state, scientists use viruses carrying DNA, which then becomes integrated into the cell's own DNA. But this so-called DNA-based reprogramming carries the risk of disrupting the cell's genome and leading it to become cancerous.

Now, for the first time, MIT researchers have shown that they can deliver those same reprogramming genes using RNA, the genetic material that normally ferries instructions from DNA to the cell's protein-making machinery. This method could prove much safer than DNA-based reprogramming, say the researchers, Associate Professor of Electrical and Biological Engineering Mehmet Fatih Yanik and electrical engineering graduate student Matthew Angel.

Yanik and Angel describe the method, also the subject of Angel's master's thesis, in the July 23 issue of the journal PLoS ONE.

However, the researchers say they cannot yet claim to have reprogrammed the cells into a pluripotent state. To prove that, they would need to grow the cells in the lab for a longer period of time and study their ability to develop into other cell types — a process now underway in their lab. Their key achievement is demonstrating that the genes necessary for reprogramming can be delivered with RNA.

"Before this, nobody had a way to transfect cells multiple times with protein-encoding RNA," says Yanik. (Transfection is the process of introducing DNA or RNA into a cell without using viruses to deliver them.)

In 2006, researchers at Kyoto University showed they could reprogram mouse skin cells into a pluripotent, embryonic-like state with just four genes. More recently, other scientists have achieved the same result in human cells by delivering the proteins encoded by those genes directly into mature cells, but that process is more expensive, inefficient and time-consuming than reprogramming with DNA.

Yanik and Angel decided to pursue a new alternative by transfecting cells with messenger RNA (mRNA), a short-lived molecule that carries genetic instructions copied from DNA.

However, they found that RNA transfection poses a significant challenge: When added to mature human skin cells, mRNA provokes an immune response meant to defend against viruses made of RNA. Repeated exposure to long strands of RNA leads cells to undergo cell suicide, sacrificing themselves to help prevent the rest of the body from being infected.

Yanik and Angel knew that some RNA viruses, including hepatitis C, can successfully suppress that defensive response. After reviewing studies of hepatitis C's evasive mechanisms, they did experiments showing they could shut off the response by delivering short interfering RNA (siRNA) that blocks production of several proteins key to the response.

Once the defense mechanism is shut off, mRNA carrying the genes for cell reprogramming can be safely delivered. The researchers showed that they could induce cells to produce the reprogramming proteins for more than a week, by delivering siRNA and mRNA every other day.

ScienceDaily (July 23, 2010) — "Many people," says Dr. Eeva Karjalainen, of the Finnish Forest Research Institute, Metla, "feel relaxed and good when they are out in nature. But not many of us know that there is also scientific evidence about the healing effects of nature."

Forests -- and other natural, green settings -- can reduce stress, improve moods, reduce anger and aggressiveness and increase overall happiness. Forest visits may also strengthen our immune system by increasing the activity and number of natural killer cells that destroy cancer cells.

Many studies show that after stressful or concentration-demanding situations, people recover faster and better in natural environments than in urban settings. Blood pressure, heart rate, muscle tension and the level of "stress hormones" all decrease faster in natural settings. Depression, anger and aggressiveness are reduced in green environments and ADHD symptoms in children reduce when they play in green settings.

In addition to mental and emotional well-being, more than half of the most commonly prescribed drugs include compounds derived from nature -- for example Taxol, used against ovarian and breast cancer, is derived from yew trees, while Xylitol, which can inhibit caries, is produced from hardwood bark.

Dr. Karjalainen will coordinate a session on the health benefits of forests at the 2010 IUFRO World Forestry Congress in Seoul. "Preserving green areas and trees in cities is very important to help people recover from stress, maintain health and cure diseases. There is also monetary value in improving people's working ability and reducing health care costs." she says.

Hepatitis C virus (HCV) co-infection occurs in an estimated one quarter of HIV-infected persons in Europe, Australia, and the United States.

"As use of highly active antiretroviral drugs has markedly reduced opportunistic infections, HCV-related liver disease has emerged as a leading cause of death. HIV infection adversely affects both the natural history and the treatment of hepatitis C" said Dr David L Thomas, Division of Infectious Diseases, Johns Hopkins School of Medicine, USA.

For people living with HIV (PLHIV) Hepatitis C (Hep C) is a major public health challenge that can and should be controlled.

"We have a serious condition and we have clear evidence that it can be controlled" said Dr David Thomas.

Two clear solid grounds why it is important to control HCV are: It is common and very severe.

The incidence of Hep C is scary - in Baltimore, Europe or Australia, HCV occurs in 70% to up to 100% among PLHIV who acquire infection through injecting drug use (IDU).

In India, whether it is Chennai in South India, or north-east India, Hep C rates among PLHIV who acquire HIV through injecting drug use are very similar and shocking. However there are several others who just have HCV and not HIV, said Dr David.

Hep C also infects PLHIV who acquired infection through heterosexual or homosexual routes.

60% of persons who acquire HCV go on to have chronic hepatitis infection. HCV viral load is also high if person is co-infected with HIV.

"HIV decreases response to HCV treatment - can have half of treatment outcome than HIV negative individuals" said Dr David Thomas.

HIV infection adversely affects all stages of Hep C or HCV infection.

"Risk of liver failure was higher among individuals living with HIV than those individuals who were similar with regards to HCV but HIV negative" said Dr Thomas.

"Even in places where harm reduction measures are in place, HCV continues. HCV is more transmissible than HIV, so measures to control HIV are not going to be enough, they need to be intensified" said Dr Thomas.

Very few people co-infected with HIV and HCV are currently receiving testing, and treatment for HCV.

There is a clear need for harm reduction measures to intensified and expanded, testing for HCV to be expanded and HCV treatment be made available widely.

"Let's rejoice in the fact that today we have treatments that work... what we need I the political will to go the extra mile to deliver universal access" had said J Montaner, which is so much in context to improve responses to HCV and HIV co-infection.

New Haven drug developer Achillion Pharmaceuticals Inc. is preparing clinical testing of a compound that it says could be a promising treatment with other drugs in its stable against the hepatitis C virus (HCV).

Achillion said its ACH-2928 targets the specific genetic protein (NS5A) that HCV needs to replicate itself.

Achillion plans to begin clinical testing of the ACH-2928 compound in combination with other protease inhibitors it is developing to attack HCV, officials said.

Preclinical testing has shown ACH-2928 to be very good at stopping the hepatitis C virus' replication of its RNA, a gene's chemical messenger, said Milind S. Deshpande, Achillion's chief scientific officer. It also hasn't shown any unpleasant side effects or interference with other drugs aimed at arresting HCH.

An estimated 170 million people worldwide -- with three to four million new cases each year -- are infected with hepatitis C, which causes liver inflammation and can lead to cancer of the liver or liver failure.

THE number of cases of the potentially fatal liver disease hepatitis C is set to reach record levels in the Lothians.

It is expected nearly 300 new cases will be recorded before the end of the year, the highest in a decade and taking the total number of sufferers in the area to almost 10,000.

Figures from Health Protection Scotland showed there were 69 new diagnoses in the first three months of this year.

The majority of people who test positive for the disease are thought to have contracted it through injecting drugs, but it is possible to catch it in other ways.

It has been argued that public health initiatives to get more people tested is the reason for the rise, and that many testing positive have actually had the illness for several years.

However, the increase has also been blamed on complacency among drug users about associated health risks, and what is of most concern is the estimated 4500 in the Lothians who have the disease but do not know it.

A spokeswoman for the Hepatitis C Trust in Edinburgh said: "It sounds strange but actually the more diagnoses there are, the better.

"The biggest danger is those who are off the radar. You can't afford to wait until you get ill with hepatitis C to begin the treatment - the damage to the liver can be too much.

"The NHS and the Hepatitis C Trust have been doing a lot of outreach work to get to drug users and hopefully the numbers will eventually come down once we get more people screened."

Around 14 per cent of all Hepatitis C sufferers in Scotland have died since the outbreaks of the 1970s and 1980s.

Experts predicted earlier this year that a rise in liver deaths could be recorded in future years as the infection - which can lie dormant for up to two decades - catches up with people who dabbled in drug use in their youth.

Around 1000 recorded patients in the Lothians do not know how they caught it, while 300 cited "other" reasons which can include tattoos, sexual intercourse and even inheriting it from birth from a Hepatitis C positive mother.

One city centre GP, who did not want to be named, said it was not purely down to awareness.

"There is an element of that but it's very tricky to tell," he said. "The fact is there are more needles out there than ever and still a really low level of knowledge among drug users.

"I'd be surprised if a heroin addict knew about the risks of hepatitis C."

"I FELT dirty and very confused, catapulted back to a place in time I did not want to go."

Petra Wright's life was in full swing. Working as a marketing officer with one of the Capital's leading financial institutions, she was successful, happily married and the proud mum of a teenage son.

So when her doctor told her the joint-pain, fatigue and depression she had recently been feeling were the result of a life-limiting blood virus - Hepatitis C - her knees nearly buckled beneath her.

She knew why she had it - the result of drug taking some 20 years beforehand when she was a rebellious youth who "knew everything, but in reality, absolutely nothing".

"I was very emotional," the 56-year-old explains. "I felt as though I had just fallen off the edge of the doctor's desk."

Like many people who contract Hepatitis C, Petra did so because of injecting drugs, inheriting the virus through blood-to-blood contact with an infected user, most likely through a syringe.

She is the first to admit how "stupid" her actions were - and nobody will live with the consequences more painfully than herself.

But as new statistics today reveal that cases of Hepatitis C across the Lothians are rising - and set to reach a record 10-year high - she is fighting for better awareness of the condition. Society simply does not know enough about Hepatitis C, she argues, but its existence affects everyone.

Drug users are not the only people at risk of getting the virus - any activity that can involve blood-to-blood contact may put someone in danger.

The list of scenarios is therefore long - getting a tattoo or piercing, a blood transfusion or acupuncture, or working in a hospital, are just a few examples.

Back in 2002, actress and model Pamela Anderson, the former star of Baywatch, revealed she had Hepatitis C, claiming she caught it from her ex-husband, musician Tommy Lee Jones, pictured far right with Anderson, after they shared a tattoo needle.

Other cases have also been revealed in recent years by former midwives who believe they were infected at work.

"The main transmission route is definitely drugs," Bo'ness-based Petra explains. "But it does not stop there. Any blood-to-blood contact can put someone at risk.

"In Asia, Hepatitis C is often spread through religious practices, such as circumcisions. I know one woman who can only attribute getting the virus to a 'dodgy tattoo' she had done.

It's not just needles that have to be clean - a pot of ink can carry the virus if a contaminated needle has been dipped in it."

If Petra, who is now the Scottish officer for the Hepatitis C Trust, could change anything about the public's perception of the virus, it would be the common misunderstanding that it is only the "drug users' disease".

"Sadly, it's not just the general public who can make that assumption though," she sighs. "It can be health professionals too. I have met people who, as soon as they were diagnosed with the virus, were asked if they used drugs - it was the first question posed to them.

"Others were advised by medics to be careful who they told about their condition. It's like being told to keep a secret.

"Hepatitis C certainly isn't talked about enough - there is a stigma about it. One thing that does not seem to come across as a result is that in the UK there are three times more people with Hepatitis C than with HIV, yet the concentration remains on HIV. We need to focus on getting rid of Hepatitis C."

Although there is no vaccine, Hepatitis C can be cured through treatment and the earlier the virus is diagnosed, and the earlier treatment starts, the better chances of recovery are.

Andrew Orr should know. The 46-year-old, also from Bo'ness, found out he had the virus just under four years ago. He had always had a suspicion. Many years of on-and-off drug abuse increased the likelihood, yet he refused to face up to the fact something was wrong.

Eventually, with multiple health problems, including poor concentration, fatigue and joint pains, he went to the doctor and was dealt the devastating blow of a diagnosis.

"I had waited so long that my liver was already diseased and I had gall bladder and other problems," he says. "I wasn't really surprised to be told I had the virus. I took a long time trying to ignore the facts and looked to blame something else for my health problems."

Andrew was one of the lucky ones as doctors began treating his condition immediately for a year, through gruelling injections and medication, allowing him to be clear of the virus.

"I think there is still a lot of stigma about Hepatitis C that isn't deserved," he says. "So to anyone reading this, worried they may have the virus, I say to them there is a cure, go and be tested and don't ever leave it as long as I did."

Petra's situation is somewhat different. Like many sufferers of the condition, it took many decades for any symptoms of the virus to show. The result was she lived with it with 20 years, unaware, raising a son, developing a career and enjoying life with her much-loved husband.

"The thought I may have passed the virus on to my son was my biggest concern. It was just terrible," she says. "Thankfully he was fine. My husband and I decided not to tell many people at first though and just kept it within the family.

Eventually, the more I said 'Hepatitis C', the easier it got."

Petra was told back in 1991 she was carrying Hepatitis C antibodies, but a full diagnosis was not made until 2003. A year later she started treatment, but is yet to be have any success.

She is to begin her next course of drugs soon, a programme which will last 48 weeks.

"What would it like to have the all clear?" she sighs. "Absolutely wonderful. It would be great not to be infectious to anyone any more."

Any treatment for the virus does not come without risks. Although Petra already suffers from memory loss and depression as a result of the condition, her last course of treatment resulted in a psychotic side-effect, something doctors are planning to address this time around through medication.

For now, Petra looks ahead to the future, quietly hopeful there will good news for her around the corner.

And she hopes awareness of the condition will continue to grow.

"The drug-user perception concerns me right now," she says.

"For example, I got Hepatitis C more than 30 years ago. It is not right to keep labelling people for the folly of their youth."

The facts behind a treatable disease

IT is a blood-borne virus affecting many parts of the body - including the brain and the digestive system - but mainly attacks the liver, often leading to cancer, liver disease, or death.

The virus was only discovered in the 1980s and there are still aspects that are not fully understood.

Around 170 million people worldwide are thought to have Hepatitis C.

A common misunderstanding of the virus is that sufferers cannot be cured - they certainly can be.

Treatment success rates are as high as 80 per cent, but there is not yet a vaccine.

HIV epidemic at a crossroads as delegates, buoyed by scientific progress, confront the possibility of stagnant funding for program scale-up

23 July 2010 [Vienna, Austria]–The biennial meeting of the global AIDS community concluded today with clear evidence of tangible progress in HIV research and programme scale up, yet facing an urgent need for increased resources, the protection of human rights, and broader use of scientifically sound prevention strategies. Delegates and organizers depart Vienna – where the conference opened 18 July under the theme of Rights Here, Right Now -- with a renewed commitment to push for securing universal access to HIV prevention, care, treatment and support.

"International governments say we face a crisis of resources, but that is simply not true: The challenge is not finding money, but changing priorities. When there is a Wall Street emergency or an energy crisis, billions upon billions of dollars are quickly mobilized. People's health deserves a similar financial response and much higher priority," said Dr. Julio Montaner, AIDS 2010 Chair, President of the International AIDS Society and Director of the B.C. Centre for Excellence in HIV/AIDS in Vancouver, Canada. "Billions of people stand in solidarity with us in our drive for universal access. We must rally their support behind Michel Sidibé's Prevention Revolution and Treatment 2.0 initiative and UNAIDS to ensure that world leaders do not turn their backs on their pledge to reach the goal of universal access."

AIDS 2010 drew 19,300 participants from 193 countries. The week-long programme featured 248 sessions covering science, community and leadership. The conference was supported by 770 volunteers from Vienna and elsewhere.

"The legacy of Vienna is the proof that we can scale up treatment and prevention to all those in need," said Dr. Brigitte Schmied, AIDS 2010 Local Co-Chair and President of the Austrian AIDS Society. "Despite the formidable obstacles in our path, we leave here with renewed energy to maintain momentum."

Vienna Declaration

By the close of the conference, more than 12,725 individuals had signed the Vienna Declaration, the official declaration of the XVIII International AIDS Conference. On Thursday, the First Lady of Georgia, H.E. Sandra Elisabeth Roelofs, signed the declaration, adding her voice to the call for more rational and scientifically sound drug policies to strengthen HIV prevention for people who use drugs.

Closing Features Examination of Conference Issues

Rapporteur reports in each of the scientific tracks and programme areas examined the key issues addressed by conference delegates over the past week and will play an important role in evaluating the conference and its impact.

The Closing Session featured a video address by South African Archbishop Desmond Tutu, remarks by Rachel Ong, Chair of the Global Network of People Living with HIV, and Patricia Perez, Chair of the International Steering Committee of the International Community of Women Living with HIV/AIDS. Montaner and Incoming IAS President Elly Katabira, Professor of Medicine at Makerere University in Uganda, presented the first IAS Presidential Award to Jack Whitescarver of the U.S. National Institutes of Health and Katabira gave an inaugural address.

At the conclusion of the Closing Session, representatives of the AIDS 2010 local partners officially transferred the International AIDS Conference globe from Vienna to Washington, DC, which will host the XIX International AIDS Conference in July 2012. Accepting the globe for DC were AIDS 2012 Local Co-Chair Dr. Diane Havlir and representatives of the AIDS 2012 local partners.

Earlier today, delegates heard from three plenary speakers.

HIV and Incarceration: Prisons and Detention

The first of today's plenary presentations featured two speakers. Dmytro Shermebey (Ukraine) of the All-Ukranian Network of PLHA offered a powerful account of his personal fight for survival during a nine-year prison sentence served in a Ukranian jail where he contracted HIV, hepatitis and tuberculosis. He survived because he wanted to prove that prisoners are humans who have a right to life, respect, understanding, help and protection.

UN Special Rapporteur on Torture, Manfred Nowak, said there is an urgent need for a comprehensive reform of the criminal justice and prison system to ensure an adequate response to the HIV/AIDS epidemic and detainees' human rights. The prevalence of HIV/AIDS and TB in prisons and the measures authorities take to deal with it, impact – and often violate – detainees' human rights. It is often forgotten that while prisoners are denied their right to liberty, they have not abrogated their other rights, such as the right to health or the right to freedom from cruel and unusual punishment.

For several reasons, prisons are characterized by particularly high HIV prevalence and are conducive to the spread of the epidemic. The transmission of HIV largely is due to risk behaviour and the failure of states to provide harm reduction measures. Evidence-based interventions, such as voluntary HIV testing and counseling and the provision of condoms, needles, syringes and opioid substitution therapy, would provide effective means to contain the spread of HIV. However, locked up behind prison walls, the fate of detainees is largely forgotten by society. The mere fact that about 30 million detainees enter and leave prisons every year highlights that prisoners' health is a pressing public health issue.

Care and Support: Integral to Comprehensive Care

Elizabeth Gwyther (South Africa) of the Hospice and Palliative Care Association of South Africa called for the integration of HIV treatment, care and support programmes to ensure comprehensive HIV care to meet the needs of PLHIV. Gwyther described the experience of PLHIV beginning at the time they present to health care providers, often because of an opportunistic infection, highlighting the complex interventions and continuity of care they need to maintain their health and mitigate HIV's impact on their socio-economic status. She noted that palliative and supportive care should not be reserved for end-of-life care because it plays an important role in promoting health restoration.

Gwyther also spoke about the experiences of community care workers who work on the front-line of the community response to HIV, saying that many are undervalued and do not receive the recognition they deserve. In addition to a policy for integrated HIV care, she called for governments and donors to provide accessible funding to support the community-led response to HIV/AIDS.

Hepatitis C: Cure and Control, Right Now

Dr. David Thomas (United States) of the Johns Hopkins School of Medicine said HIV and HCV coinfection is a serious and common problem, particularly among people who acquired HIV through drug use, and causes liver disease that is not sufficiently controlled by antiretroviral therapy. HIV/HCV co-infected persons die at a much higher rate than people with only one of the two infections, and liver failure is now the second leading cause of death among PLHIV on antiretroviral therapy.

While there are major challenges in addressing hepatitis C, HCV infection is curable and major improvements in treatment are expected within the year. Thomas called for scale-up of hepatitis C testing, particularly among PLHIV, and new ways to integrate HCV treatment with comprehensive HIV health and wellness services. Major challenges to an effective scale-up exist as HCV screening is uncommon and engaging people who use drugs in traditional medical care can be difficult.

AIDS 2010 is convened by the IAS, the world's leading independent association of HIV professionals, in partnership with a number of international, regional and local partners. International partners for AIDS 2010 include:

•Joint United Nations Programme on HIV/AIDS (UNAIDS), including its co-sponsors, the World Health Organization (WHO) and the United Nations Office on Drugs and Crime (UNODC)
•International Council of AIDS Service Organizations (ICASO)
•Global Network of People Living with HIV/AIDS (GNP+)/International Community of Women Living with HIV/AIDS (ICW)
•World YWCA
•Caribbean Vulnerable Communities Coalition (CVC)

Local and regional partners for AIDS 2010 include local scientific leadership and:

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